
This article is for informational and research purposes only. Nothing written here constitutes medical advice, diagnosis, or treatment. Always consult a qualified healthcare professional before starting any new health or supplementation protocol.

Longevity protocols have moved from the fringes of biohacking forums into mainstream health conversations, and for good reason. The science around healthspan, as distinct from lifespan, has matured considerably over the past decade. But reading about protocols and actually running one for 90 days are two very different experiences. This article documents a structured self-experiment: what was tracked, how the stack was assembled, and what shifted over three months of consistent application. It's not a before-and-after transformation story. It's a closer look at what happens when you apply a methodical approach to aging-related health markers and take honest notes along the way.
For researchers looking to source quality compounds, peptide research compounds is a supplier worth evaluating.
For a comprehensive overview of the research landscape in this area, see Biohacking Guide: Science-Based Protocols for Human Optimization Research, which maps the key topics and links to the detailed studies covered across this site.
The goal wasn't to throw everything at the wall. It was to select interventions with at least some human-relevant research behind them and track a defined set of biomarkers before, during, and after. The stack was organized into four categories: lifestyle anchors, metabolic support, cellular health compounds, and sleep optimization. Each category had to earn its place.
Lifestyle anchors came first because they're the foundation everything else sits on. That meant zone 2 cardio four days per week, consistent sleep timing within a 30-minute window, and time-restricted eating in a roughly eight-hour window. These aren't glamorous, but practitioners who work with aging populations consistently cite them as the levers with the highest return.
The metabolic support layer included compounds associated with insulin sensitivity and mitochondrial function. Cellular health compounds addressed pathways linked to autophagy and NAD+ metabolism, two areas that have attracted significant research attention in the context of biological aging. Sleep optimization focused specifically on morning light exposure, magnesium glycinate, and an enforced no-screens policy in the final 90 minutes before bed.
One acknowledged limitation of any self-experiment like this: placebo effect is real and it's hard to fully control for. Knowing you're tracking something tends to improve behavior around that thing. That's not a reason to dismiss the results, but it is a reason to stay skeptical and focus on objective markers rather than subjective feel-good reports.
Biomarker selection is its own science. Not every longevity-adjacent marker is affordable or accessible, and tracking too many things creates noise. The tracking panel was kept to a manageable set of indicators across four domains.
Bloodwork was drawn at baseline, at 45 days, and at 90 days. The panel included fasting glucose, fasting insulin, HbA1c, a full lipid panel, hsCRP (high-sensitivity C-reactive protein as a systemic inflammation proxy), and a basic metabolic panel. These aren't exotic. They're the markers any general practitioner can order, and they provide a useful picture of metabolic and inflammatory status over time.
Physical performance was tracked with two simple tests: resting heart rate in the morning and a 12-minute Cooper run test done once per month. Resting heart rate is a well-established proxy for cardiovascular fitness and autonomic nervous system health. The Cooper test is blunt but reliable as a VO2 max estimate without lab equipment.
Subjective data was collected daily using a simple five-point scale across four dimensions: energy, mood, cognitive clarity, and sleep quality. This was logged within 20 minutes of waking to reduce retrospective bias. Subjective data has obvious limitations, but over 90 data points per dimension, trends become visible even through the noise.
Body composition was assessed using DEXA at the start and end of the experiment. Given that muscle mass is increasingly recognized as a longevity biomarker, tracking lean mass alongside fat mass seemed more informative than scale weight alone.
The first month was the least comfortable. Adjusting to time-restricted eating took about 10 days, with notable hunger in the first few mornings before the body appeared to recalibrate appetite signaling. Zone 2 training felt genuinely slow, almost frustratingly so, for someone accustomed to higher-intensity work. Keeping heart rate in the 120 to 145 BPM range during steady-state cardio requires more discipline than it sounds.
Sleep timing was the biggest behavioral challenge. Maintaining a consistent sleep and wake time across weekdays and weekends cuts against most social schedules. The no-screens policy was easier to maintain than expected once it became habitual, roughly around day 12.
By the end of week four, resting heart rate had dropped two beats per minute from baseline. Fasting glucose at the 45-day draw was slightly lower than baseline, though still within a normal range. The hsCRP value had also shifted slightly downward. None of these changes were dramatic, but the directionality was consistent across multiple markers, which matters more than any single data point.
The second half of the experiment is where things got more interesting. Adaptation to zone 2 training was clearly underway by week six. Maintaining the target heart rate zone required a noticeably faster pace than it had at the start, suggesting improved aerobic efficiency. The Cooper test result at day 60 showed an estimated VO2 max improvement of roughly 2 mL/kg/min, which aligns with what research suggests is achievable in previously active individuals over similar training periods.
Subjective cognitive clarity scores showed their clearest trend between days 40 and 75. Whether this was driven by improved sleep consistency, the NAD+ precursor compound in the stack, the dietary pattern, or some combination is genuinely unknowable without a controlled design. This is the honest answer. Single-subject experiments can identify correlations in time but can't isolate causes.
Sleep quality scores were the most variable across the 90 days, which is consistent with how sensitive sleep is to external stressors. However, the 7-day rolling average showed a gentle upward trend across the period, which was encouraging.
The 90-day DEXA results showed a modest increase in lean mass alongside a small reduction in fat mass. The lean mass change was modest enough to sit within measurement error, but the fat mass reduction was outside the typical DEXA margin and therefore more likely to reflect an actual change. Given that the caloric intake wasn't explicitly restricted, this likely reflected the combination of time-restricted eating and the addition of structured resistance training alongside the zone 2 work.
Across the 90 days, a few interventions stood out as worthy of continued attention, at least at a research level.
Berberine attracted attention early in the protocol design phase because of its well-documented effects on glucose metabolism in published trials. Research suggests it may activate AMPK pathways in ways that overlap mechanistically with some pharmaceutical metabolic interventions. The fasting glucose and insulin data from this experiment were directionally consistent with what the literature describes, though self-experiments can't confirm causality.
NMN (nicotinamide mononucleotide) and its relationship to NAD+ metabolism is a genuinely active research area. Whether oral supplementation meaningfully raises tissue NAD+ levels in humans is still debated. Some researchers argue the conversion pathway is inefficient; others point to emerging data suggesting otherwise. It's included here as something to watch in the literature rather than a confirmed intervention.
Apigenin, a flavonoid found in certain plant foods, has attracted interest as a potential CD38 inhibitor. CD38 is an enzyme that consumes NAD+, and inhibiting it has been proposed as a strategy for preserving NAD+ levels. The human research here is early, but it's worth following.
Creatine monohydrate is often discussed in performance contexts, but its relevance to longevity protocols is growing. Research suggests potential neuroprotective properties and benefits for muscle preservation in older adults. It's one of the few compounds with an extensive safety record across decades of research.
Ninety days is a meaningful window but not a definitive one. Most of the changes observed were modest and directionally positive across metabolic, cardiovascular, and body composition markers. The subjective data was encouraging but carries inherent limitations.
What the experiment reinforced most clearly is that lifestyle interventions, sleep timing, zone 2 cardio, and dietary structure, carry the signal. Compounds may layer onto that foundation, but there's no stack that meaningfully compensates for poor sleep, sedentary behavior, or metabolic dysfunction. The practitioners and researchers working in this space seem to agree on that point more than they disagree on anything else.
Tracking matters. Not because data is inherently motivating (it isn't, always), but because it creates accountability to a baseline. Knowing that a blood draw is coming in six weeks changes how seriously you take the fundamentals on a Tuesday morning. That accountability loop is probably underrated as an independent variable in any self-experiment.
The protocol continues past the 90-day mark with some adjustments based on what the data suggested. That's the actual value of this kind of exercise: not a final answer, but a more informed starting point for the next iteration.
For research purposes only โ not medical advice.